Cardiac organoids effectively model myocardial infarction features and hypoxia-enhanced doxorubicin cardiotoxicity, aiding drug screening applications.
Human cardiac organoids can successfully model the structural and functional hallmarks of myocardial infarction and drug-induced cardiotoxicity, offering a novel platform for drug screening.
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Environmental factors are the largest contributors to cardiovascular disease. Here we show that cardiac organoids that incorporate an oxygen-diffusion gradient and that are stimulated with the neurotransmitter noradrenaline model the structure of the human heart after myocardial infarction (by mimicking the infarcted, border and remote zones), and recapitulate hallmarks of myocardial infarction (in particular, pathological metabolic shifts, fibrosis and calcium handling) at the transcriptomic, structural and functional levels. We also show that the organoids can model hypoxia-enhanced doxorubicin cardiotoxicity. Human organoids that model diseases with non-genetic pathological factors could help with drug screening and development.
Richards et al. (Mon,) reported a other. Cardiac organoids effectively model myocardial infarction features and hypoxia-enhanced doxorubicin cardiotoxicity, aiding drug screening applications.